De Marinis L, Mancini A, Valle D, Bianchi A, Gentilella R, Milardi D, Mascadri C, Giustina A
Institute of Endocrinology and Department of Internal Medicine II, Catholic University, Rome, Italy.
Metabolism. 2000 Feb;49(2):155-9. doi: 10.1016/s0026-0495(00)91091-6.
Galanin (GAL) elicits growth hormone (GH) release in normal subjects through interaction with hypothalamic somatostatin. GAL also stimulates GH-releasing hormone (GHRH) secretion in vitro. In rats, GAL is able to stimulate prolactin (PRL) release, but this effect is not clear in humans. We have thus investigated GAL effects on GH and PRL release in patients with anorexia nervosa (AN), known to have altered regulation of the GH-insulin-like growth factor axis and PRL dynamics, and compared the effects of GHRH and GAL on GH and PRL secretion in AN and normal healthy subjects. Eight women with AN (15 to 27 years; body mass index [BMI], 17 to 19.5 kg/m2) were treated with (1) GHRH 50 microg intravenous (IV) injection, (2) porcine GAL 500 microg infusion from -10 to +30 minutes, and (3) 135-minutes saline infusion as a control, respectively. Both peptides induced a significant increase in plasma GH in AN patients (peak level, 27.41 +/- 5.50 microg/L after GAL and 18.97 +/- 2.67 microg/L after GHRH). When data for AN patients and the control group were compared, GH peak levels after GAL were significantly higher in AN patients (27.41 +/- 5.50 v 13.64 +/- 2.32 microg/L), while GH peak levels after GHRH were not different between the 2 groups (18.97 +/- 2.67 v 15.98 +/- 3.88 microg/L). PRL levels significantly increased after both GHRH (peak, 11.70 +/- 2.80 microg/L) and GAL (peak, 18.02 +/- 5.10 microg/L) treatment in AN patients, but not in normal subjects. We conclude that GAL stimulates exaggerated GH release in AN patients as compared with normal controls, suggesting a dual hypothalamic interaction via both an increase in endogenous GHRH and a decrease in somatostatin secretion. Finally, GAL may act as a PRL secretagogue in AN patients.
甘丙肽（GAL）通过与下丘脑生长抑素相互作用，促使正常受试者释放生长激素（GH）。GAL在体外也能刺激生长激素释放激素（GHRH）的分泌。在大鼠中，GAL能够刺激催乳素（PRL）释放，但在人类中这种作用尚不清楚。因此，我们研究了GAL对神经性厌食症（AN）患者GH和PRL释放的影响，已知这些患者的GH - 胰岛素样生长因子轴调节和PRL动态发生改变，并比较了GHRH和GAL对AN患者及正常健康受试者GH和PRL分泌的影响。8名患有AN的女性（年龄15至27岁；体重指数[BMI]，17至19.5kg/m²）分别接受以下治疗：（1）静脉注射50μg GHRH，（2）在-10至+30分钟内输注500μg猪GAL，（3）输注135分钟生理盐水作为对照。两种肽均使AN患者血浆GH显著升高（GAL后峰值水平为27.41±5.50μg/L，GHRH后为18.97±2.67μg/L）。当比较AN患者和对照组的数据时，GAL后AN患者的GH峰值水平显著更高（27.41±5.50对13.64±2.32μg/L），而GHRH后两组的GH峰值水平无差异（18.97±2.67对15.98±3.88μg/L）。AN患者在接受GHRH（峰值，11.70±2.80μg/L）和GAL（峰值，18.02±5.10μg/L）治疗后PRL水平均显著升高，但正常受试者未出现这种情况。我们得出结论，与正常对照组相比，GAL刺激AN患者释放过量的GH，提示通过内源性GHRH增加和生长抑素分泌减少的双重下丘脑相互作用。最后，GAL可能在AN患者中作为PRL促分泌素起作用。
